Acne vulgaris is a chronic inflammatory disease of the skin which can cause an undesirable appearance on the face, back and other areas of the body. The skin comprises sebaceous glands which secrete sebum, an oily substance which is a mixture of fat and the debris of dead fat-producing cells. These cells are constantly replaced by new growth at the base of the sebaceous glands. In humans, sebaceous glands are primarily found in association with hair follicles but also occur in hairless areas of the skin, except for the palms of the hand and soles of the feet. A pilosebaceous unit consists of a sebaceous gland, a hair shaft, a hair follicle, and an erector pili muscle which causes the hair to stand up when it contracts. The follicle comprises cells which are involved in hair production and corneocytes of the epidermal layer of the skin lining the follicles. Generally the sebum is deposited on the hairs inside the follicles and is brought up to the surface of the skin along the hair shaft. In hairless areas, the sebum surfaces through ducts.
While sebum serves the purpose of lubricating and protecting the hair and skin and preventing drying and irritation of membranes, it may also be detrimental if it is blocked from exiting the follicle or duct. In acne vulgaris, desquamated (shed) follicular cells and sebum may form a plug which blocks the excretion of sebum from the follicle. This manifests as a “whitehead” also called a closed comedone. Though different theories have been proposed for the dark color of another type of skin blemish commonly known as a “blackhead,” it has been reported that oxidized sebum oil (perhaps mixed with other substances such as melanin) may be responsible. This oxidized oil may harden in the follicle, contributing to the plugging of the normal sebum drainage of the follicle.
Propionibacterium acnes, is an anaerobic bacterium and has been reported to be the primary pathogenic agent involved with the development of inflammatory acne and comedogenesis. The plugged follicle provides a favorable anaerobic environment complete with a nourishment source (sebum) for the organism. Overgrowth of Propionibacterium acnes has been reported to cause destruction of the lining of the follicle, which allows follicular material to enter the dermis
Propionibacterium acnes hydrolyzes the oil in the sebum, thereby causing the release of free fatty acids. This release of free fatty acids into the surrounding tissue due to rupture of the sebaceous gland causes inflammation. Certain terminology has been generally ascribed to skin blemishes resulting from inflammation, while recognizing that categorization may be subjective to a certain extent. A “pustule” is terminology ascribed to a skin blemish resulting from inflammation very near the surface of the skin. A “pimple” is terminology ascribed to a skin blemish resulting from deeper inflammation. A “cyst” is terminology ascribed to a skin blemish resulting from still deeper inflammation.
While many approaches to acne treatment have been reported, some have advocated use of a systemic or topical agent to address the overgrowth of Propionibacterium acnes. 
Systemic therapy requires prescription antibiotics, such as erythromycin, tetracyclines, and clindamycin, however in recent times physicians have become reluctant to over-prescribe antibiotics because resistance may be developed by not only acne-causing bacteria but other bacteria which are the causative agents of other more serious diseases. Furthermore, systemic administration may cause systemic side effects, as relatively high levels of the drug must circulate throughout the entire body.
Topical antibiotics which have been utilized to attempt to inhibit the overgrowth of Propionibacterium acnes are clindamycin, erythromycin, tetracycline, and metronidazole. Each of these topical antibiotics reportedly cause side effects and widespread use also contributes to the risk of bacterial resistance.